Myelin oligodendrocyte glycoprotein autoantibody (MOG-IgG) (MOG-IgG)

Myelin oligodendrocyte glycoprotein (MOG) autoantibodies are pathogenic immunoglobulins, primarily of the IgG1 subclass, that target the extracellular IgV domain of the MOG protein expressed on the surface of myelin sheaths and oligodendrocytes in the central nervous system (Reindl & Waters, Nat Rev Neurol, 2019). These autoantibodies are the defining feature of MOG antibody-associated disease (MOGAD), a neuroinflammatory condition distinct from multiple sclerosis and AQP4-positive neuromyelitis optica spectrum disorder (Banwell et al., Lancet Neurol, 2023). Upon binding to MOG, these antibodies can activate the classical complement pathway and induce antibody-dependent cellular cytotoxicity, leading to demyelination and axonal damage (Peschl et al., Mol Cell Neurosci, 2017). Clinical manifestations typically include optic neuritis, transverse myelitis, and acute disseminated encephalomyelitis (Jarius et al., J Neuroinflammation, 2018). Therapeutic strategies focus on reducing the levels of these pathogenic antibodies through B-cell depletion (e.g., rituximab, inebilizumab), inhibition of the neonatal Fc receptor (FcRn) to accelerate IgG degradation (e.g., rozanolixizumab), or physical removal via plasma exchange (Whittam et al., Front Neurol, 2020). Monitoring serum MOG-IgG titers using live cell-based assays is essential for accurate diagnosis and for assessing the risk of disease relapse (Reindl & Waters, Nat Rev Neurol, 2019).

Other names

Anti-MOG antibodyMOG antibodyMyelin oligodendrocyte glycoprotein antibodyMOG-AbAnti-myelin oligodendrocyte glycoprotein

Therapeutic strategies focus on reducing the concentration or pathogenic activity of MOG-specific autoantibodies through B-cell depletion (targeting CD20 or CD19), inhibition of the neonatal Fc receptor (FcRn) to enhance IgG clearance, or direct removal via plasma exchange (Whittam et al., Front Neurol, 2020; UCB, ClinicalTrials.gov).